名古屋大学 · 의학
유노야마 요시히사 교수의 연구실은 뇌의 KNDy 신경세포(키스프틴, 네오키나인 B, 덴포르민 A를 발현하는 세포)가 생식 호르몬 분비의 핵심 조절자로 작용하는 메커니즘을 규명하는 데 초점을 맞추고 있습니다. 특히 펄스 형태의 GnRH 분비를 조절하는 신경 회로와 이들이 청소년기 발달 및 생식 기능 유지에 미치는 영향을 동물 모델(마우스, 쥐, 돼지 등)을 통해 연구하고 있습니다. 또한, 생식 기능과 관련된 신경-호르몬 상호작용, 특히 키티프틴-수용체 신호전달 경로의 기능적 역할을 분자생물학적·해부학적 접근으로 탐구하고 있습니다.
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
The gonadotropin-releasing hormone (GnRH) pulse is fundamental for mammalian reproduction: GnRH pulse regimens are needed as therapies for infertile women as continuous GnRH treatment paradoxically inhibits gonadotropin release. Circumstantial evidence suggests that the hypothalamic arcuate KNDy neurons expressing <u>k</u>isspeptin (encoded by <i>Kiss1</i>), <u>n</u>eurokinin B (encoded by <i>Tac3</i>), and <u>d</u><u>y</u>norphin A serve as a GnRH pulse generator; however, no direct evidence is
Kisspeptin, encoded by the Kiss1 gene, has attracted attention as a key candidate neuropeptide in controlling puberty and reproduction via regulation of gonadotrophin-releasing hormone (GnRH) secretion in mammals. Pioneer studies with Kiss1 or its cognate receptor Gpr54 knockout (KO) mice showed the indispensable role of kisspeptin-GPR54 signalling in the control of animal reproduction, although detailed analyses of gonadotrophin secretion, especially pulsatile and surge-mode of luteinising horm
The present study was conducted to determine the morphological and functional interaction between kisspeptin and gonadotrophin-releasing hormone (GnRH) neuronal elements at the median eminence in female rats to clarify a possibility that kisspeptin directly stimulates GnRH release at the nerve end. A dual immunoelectron microscopic study of kisspeptin and GnRH showed that the kisspeptin-immunoreactive nerve element directly abutted the GnRH-immunoreactive nerve element, although no obvious synap
Increasing evidence accumulated during the past two decades has demonstrated that the then-novel kisspeptin, which was discovered in 2001, the known neuropeptides neurokinin B and dynorphin A, which were discovered in 1983 and 1979, respectively, and their G-protein-coupled receptors, serve as key molecules that control reproduction in mammals. The present review provides a brief historical background and a summary of our recent understanding of the roles of hypothalamic neurons expressing kissp
Pubertal onset is thought to be timed by an increase in pulsatile gonadotropin-releasing hormone (GnRH)/gonadotropin secretion in mammals. The underlying mechanism of pubertal onset in mammals is still an open question. Evidence accumulated in the last 15 years suggests that kisspeptin/neurokinin B/dynorphin A (KNDy) neurons in the hypothalamic arcuate nucleus play a key role in pubertal onset by triggering pulsatile GnRH/gonadotropin secretin in mammals. Specifically, KNDy neurons are now consi
Porcine endometrial cells (a mixture of epithelial, stromal, and glandular cells) were examined for the presence of oxytocin (OT) receptors using a cell culture system and a 125I-labeled OT antagonist. Binding specificity was tested in displacement studies with various related peptides. Scatchard analyses revealed the presence of a binding site with a dissociation constant (Kd) = 0.9 nM and a capacity of 1.9 fmol/10(5) cells. These cells, which were obtained from prepubertal gilts and thus had n
Estrogen produced by ovarian follicles plays a key role in the central mechanisms controlling reproduction via regulation of gonadotropin-releasing hormone (GnRH) release by its negative and positive feedback actions in female mammals. It has been well accepted that estrogen receptor α (ERα) mediates both estrogen feedback actions, but precise targets had remained as a mystery for decades. Ever since the discovery of kisspeptin neurons as afferent ERα-expressing neurons to govern GnRH neurons, t
Kisspeptin, encoded by KISS1/Kiss1 gene, is now considered a master regulator of reproductive functions in mammals owing to its involvement in the direct activation of gonadotropin-releasing hormone (GnRH) neurons after binding to its cognate receptor, GPR54. Ever since the discovery of kisspeptin, intensive studies on hypothalamic expression of KISS1/Kiss1 and on physiological roles of hypothalamic kisspeptin neurons have provided clues as to how the brain controls sexual maturation at the onse
Kisspeptin, identified as a natural ligand of GPR54 in 2001, is now considered as a master regulator of puberty and subsequent reproductive functions in mammals. Our previous studies using Kiss1 knockout (KO) rats clearly demonstrated the indispensable role of kisspeptin in gonadotropin-releasing hormone (GnRH)/gonadotropin secretion. In addition, behavioral analyses of Kiss1 KO rats revealed an organizational effect of kisspeptin on neural circuits controlling sexual behaviors. Our studies usin
Kisspeptin (also known as metastin), a hypothalamic peptide, has attracted attention as a key molecule in the release of gonadotrophin-releasing hormone (GnRH) in various mammalian species, such as rodents, sheep and primates. Two populations of kisspeptin neurones in the brain may control two modes of GnRH release to time the onset of puberty and regulate oestrous cyclicity in rats and mice. One population of kisspeptin neurones, located in the anteroventral periventricular nucleus, appears to
Pulsatile secretion of gonadotrophin-releasing hormone (GnRH)/luteinising hormone is indispensable for the onset of puberty and reproductive activities at adulthood in mammalian species. A cohort of neurones expressing three neuropeptides, namely kisspeptin, encoded by the Kiss1 gene, neurokinin B (NKB) and dynorphin A, localised in the hypothalamic arcuate nucleus (ARC), so-called KNDy neurones, comprises a putative intrinsic source of the GnRH pulse generator. Synchronous activity among KNDy n
Hypothalamo-pituitary-gonadal axis has been recognized as a functional unit orchestrating reproductive performance in mammals. The mechanism governing puberty onset, however, is still one of the great mysteries of biology. The present article reviews previous studies over the last century, which gradually elucidated the brain mechanism controlling puberty onset in mammals along with the discovery of gonadotrophins and the gonadotrophin-releasing hormone and the establishment of the concept for t
After the discovery of hypothalamic kisspeptin encoded by the Kiss1 gene, the central mechanism regulating gonadotropin-releasing hormone (GnRH) secretion, and hence gonadotropin secretion, is gradually being unraveled. This has increased our understanding of the central mechanism regulating puberty and subsequent reproductive performance in mammals. Recently, emerging evidence has indicated the molecular and epigenetic mechanism regulating hypothalamic Kiss1 gene expression. Here we compile dat
Endogenous opioid peptides have attracted attention as critical neuropeptides in the central mechanism regulating female reproduction ever since the discovery that arcuate dynorphin neurons that coexpress kisspeptin and neurokinin B (NKB), which are also known as kisspeptin/neurokinin B/dynorphin (KNDy) neurons, play a role as a master regulator of pulsatile gonadotropin-releasing hormone (GnRH) release in mammals. In this study, we first focus on the role of dynorphin released by KNDy neurons i
